Cryptotanshinone Inhibits Lipid Accumulation in Differentiating 3T3-L1 Preadipocytes by Down-regulating C/EBP-α, PPAR-γ, FAS, Perilipin A, and STAT-3
- Author:
Yu Kyoung PARK
1
;
Byeong Churl JANG
Author Information
1. Department of Molecular Medicine, Keimyung University School of Medicine, Daegu, Korea. lympia2012@naver.com
- Publication Type:Original Article
- Keywords:
Cryptotanshinone;
CCAAT/enhancer-binding protein-α;
Perilipin A;
Perilipin A transcription-3
- MeSH:
3T3-L1 Cells;
Adipocytes;
Adipogenesis;
Lipid Droplets;
Obesity;
Peroxisomes;
Phenotype;
Phosphorylation;
Transducers;
Triglycerides
- From:Keimyung Medical Journal
2019;38(1):1-10
- CountryRepublic of Korea
- Language:English
-
Abstract:
Differentiation of preadipocyte, also named adipogenesis, leads to the phenotype of mature adipocyte that is filled with many lipid droplets. Excessive lipid accumulation in adipocytes leads to the development of obesity. In this study, we investigated the effect of 11 different natural compounds on lipid accumulation during the differentiation of 3T3-L1 preadipocytes into 3T3-L1 adipocytes. Strikingly, among the natural compounds, cryptotanshinone at 10 µM most strongly reduced triglyceride (TG) contents in 3T3-L1 cells after 8 days of the differentiation. Furthermore, cryptotanshinone at 10 µM significantly suppressed lipid accumulation in 3T3-L1 cells after 8 days of the differentiation. Cryptotanshinone at 1 to 10 µM tested did not affect the survival of 3T3-L1 cells after 8 days of the differentiation. On mechanistic levels, cryptotanshinone time-differentially decreased the expression levels of CCAAT/enhancer-binding protein-α (C/EBP-α), peroxisome proliferator-activated receptor-γ (PPAR-γ), fatty acid synthase (FAS), and perilipin A but also the phosphorylation levels of signal transducer and activator of transcription-3 (STAT-3) during the 3T3-L1 cell differentiation. Taken together, these findings demonstrate that cryptotanshinone inhibits lipid accumulation in differentiating 3T3-L1 cells, which appears to be mediated through the reduced expression and/or phosphorylation levels of C/EBP-α, PPAR-γ, FAS, Perilipin A, and STAT-3.
